Log on/register
BioMed Central home | Journals A-Z | Feedback | Support | My details
 

This article is part of the supplement: Association for Immunotherapy of Cancer: Cancer Immunotherapy – 2nd Annual Meeting .

Open AccessOral presentation

Genetically modified natural killer cells specifically recognizing the tumor-associated antigens ErbB2/HER2 and EpCAM

C Uherek1 email, T Müller1, T Tonn1,2, B Uherek1, H-G Klingemann3 and WS Wels1

Chemotherapeutisches Forschungsinstitut Georg-Speyer-Haus, Frankfurt/Main, Germany

Institute for Transfusion Medicine and Immunohematology RCBDS, Frankfurt/Main, Germany

Section of Bone Marrow Transplant and Cell Therapy, RUSH Medical Center, Chicago, IL, USA

author email corresponding author email

from Association for Immunotherapy of Cancer: Cancer Immunotherapy – 2nd Annual Meeting
Mainz, Germany. 6–7 May 2004

Cancer Cell International 2004, 4(Suppl 1):S7doi:10.1186/1475-2867-4-S1-S7

Published: 1 July 2004

First paragraph (this article has no abstract)

The continuously growing natural killer (NK) cell line NK-92 is highly cytotoxic against malignant cells of various origin without affecting normal human cells. Based on this selectivity, the potential of NK-92 cells for adoptive therapy is currently being investigated in phase I clinical studies. To further enhance the antitumoral activity of NK-92 cells and expand the range of tumor entities suitable for NK-92-based therapies, here by transduction with retroviral vectors we have generated genetically modified NK-92 cells expressing chimeric antigen receptors specific either for the tumor-associated ErbB2 (HER2/neu) antigen or the human Epithelial Cell Adhesion Molecule (Ep-CAM). Both antigens are overexpressed by many tumors of epithelial origin. The chimeric antigen receptors consist of either the ErbB2 specific scFv(FRP5) antibody fragment or the Ep-CAM specific scFv(MOC31), a flexible hinge region derived from CD8, and transmembrane and intracellular regions of the CD3 zeta chain.


© 1999-2010 BioMed Central Ltd unless otherwise stated. Part of Springer Science+Business Media.